Public Health Agency of Canada
Symbol of the Government of Canada

Share this page

Brugia spp. - Pathogen Safety Data Sheet

SECTION I – INFECTIOUS AGENT

NAME: Brugia spp.

SYNONYM OR CROSS REFERENCE: Brugia malayi, Brugia timori, Brugia pahangi, Brugia beaveri, Brugia lepori, Brugia guyanensis, lymphatic filariasis, Timorean filariasis, Malayan filariasis, Brugian filariasis.

CHARACTERISTICS: Brugia spp. are arthropod-transmitted nematodes of the superfamily Filarioidae 1Footnote 2. Female worms measure 80 mm to 100 mm long by 240 µm to 300 µm wide, and the males are 13 mm to 20 mm long and 70 µm to 80 µm wide. The gravid females produce large numbers of embryonated eggs, and sheathed microfilariae of a size of 200 to 300 µm by 5 to 6 µm develop from ova. B. timori microfilariae are larger (more than 300 µm long). Microfilariae are located on a double-layered sheath Footnote 3, and accumulate in the pulmonary vessels during the day and into the peripheral circulation at night 1Footnote 2.

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Brugia spp. is one of the causative agents of lymphatic filariasis. Many infections remain asymptomatic despite circulating microfilariae. Clinical consequences of filarial infection are principally due to inflammatory responses to developing, mature, and dying worms. The initial manifestation of infection is often acute lymphangitis and lymphadenitis on the legs or groin Footnote 4, with fever, painful lymph nodes, edema, pruritus, acute signs of adenolymphangitis, abscesses, scars at sites of ruptured lymph nodes, and inflammation, spreading peripherally from involved lymph nodes. The most common chronic manifestation of lymphatic filariasis is swelling of the extremities or genitals due to chronic lymphatic inflammation and obstruction. Extremities become increasingly swollen, with a progression over time from pitting edema, to nonpitting edema, to sclerotic changes of the skin that are referred to as elephantiasis, which may develop from later stages of edemas Footnote 1Footnote 4Footnote 5. B. timori infections are often more severe than B. malayi infections.

EPIDEMIOLOGY: B. malayi is confined to Southeast and Eastern Asia, such as eastern India, Burma, Thailand, Vietnam, southeast Indonesia, and the Philippines Footnote 4. B. timori is found only in Timor and its adjacent islands Footnote 1Footnote 2Footnote 6. Endemicity of lymphatic filariasis has been confirmed in about 80 countries and most recent estimates suggest that filariasis infects 120 million people or 2% of the world’s population Footnote 5Footnote 6. Brugia spp. cause approximately 9-10% of these cases with the majority being caused by Wuchereria bancrofti Footnote 5Footnote 7.

HOST RANGE: Humans, mosquitoes, primates (specifically slow loris), dogs (B. malayi), cats (B. malayi), civet cats, wild felids (B. malayi), felids (B. timori), pangolins (B. timori), coatis, grisons (B. guyanensis), raccoons (B. beaveri), lynxes (B. beaveri),  rabbits (B. lepori) Footnote 1Footnote 4 Footnote 8-10.

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: Hosts are infected by the bites of infected mosquitoes. Mosquitoes deposit third-stage larvae on the skin of the host and the infective larvae penetrate the skin at the site of the bite and migrate to the lymphatic system of the host, where they mature into fecund adults worms after 3 months. The adult worms produce large numbers of microfilariae, which are released into the circulation and are picked up by a mosquito during a subsequent blood meal Footnote 5Footnote 7Footnote 11Footnote 12.

INCUBATION PERIOD: Variable; microfilariae are found in the blood 3 to 12 months after infection Footnote 4Footnote 7. The infection remains asymptomatic in many cases for years, although microfilariae are circulating in the blood Footnote 4.

COMMUNICABILITY: Transmission from human-to-human is possible Footnote 4.

SECTION III – DISSEMINATION

RESERVOIR: Humans, mosquitoes, slow loris, dogs (B. malayi), cats (B. malayi), civet cats, wild felids (B. malayi), felids (B. timori), pangolins (B. timori), raccoons (B. beaveri), coatis and grisons (B. guyanensis), lynxes (B. beaveri), and rabbits (B. lepori) Footnote 1Footnote 48-10.

ZOONOSIS: Zoonotic agents are B. malayi and B. timori Footnote 4. Humans and other hosts are infected by the bite of infected mosquitoes Footnote 4. The microfilariae ingested with the blood meal taken by mosquitoes penetrate the gut wall and migrate to the flight muscles, where they mature and become infective Footnote 7Footnote 12.

VECTORS: Mansonia spp. (B. malayi), Aedes spp. (B. malayi), and Anopheles spp. (B. timori) mosquitoes Footnote 1Footnote 2Footnote 4.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Susceptible to diethylcarbamazine (drug of choice), but has a limited action against adult worms. It is also susceptible to ivermectin, albendazole, and doxycycline Footnote 5. Doxycycline treatment depleted Wolbachia from B. malayi in infected patients Footnote 13.

DRUG RESISTANCE: No specific resistance has been reported; however, it remains a growing concern when repeated doses are administered, especially in endemic areas.

SUSCEPTIBILITY TO DISINFECTANTS: While information specific to Brugia spp. are not available other nematodes have been shown susceptible to sodium hypochlorite and ethanol Footnote 14Footnote 15, and many microorganisms are also inactivated by formaldehyde Footnote 14 and glutaraldehyde.

PHYSICAL INACTIVATION: While information specific to Brugia spp. are not available, other nematodes have been shown to been sensitive to moist heat (121°C for at least 15 min) Footnote 15 and dry heat (160°C for 1 to 2 hours) Footnote 16.

SURVIVAL OUTSIDE HOST: Unknown.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. The diagnosis is confirmed by finding microfilariae, usually in blood or lymphatic, ascitic, or pleural fluid Footnote 2Footnote 5. In addition, microfilariae may be absent, especially early in the disease progression (first 2-3 years) or with chronic obstructive disease Footnote 5. Because the appearance of the microfilariae is usually periodic, specimen collection must be properly timed. Smears are evaluated by wet mount, to identify motile parasites, and by Giemsa staining. Microfilariae may also be identified in hydrocele fluid or chylous urine. Eosinophilia is usually absent, except during acute inflammatory syndromes. Available serologic tests, including bentonite flocculation, indirect hemagglutination, ELISA, and indirect fluorescent antibody tests, may be helpful but cannot distinguish between past and active infections Footnote 2Footnote 5. Adult worms may also be found in lymph node biopsy or by ultrasound of a scrotal hydrocele or lymphedematous breast Footnote 5.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Administer appropriate drug therapy. Treatment options are somewhat limited, as no drug can fully control or reverse the disease, and treatment may cause serious acute inflammatory symptoms. Diethylcarbamazine is the drug of choice, but it cannot cure infections due to its limited action against adult worms. Asymptomatic infection and acute lymphangitis are treated with this drug, leading to a marked decrease in microfilaremia. Therapy may be accompanied by allergic symptoms, including fever, headache, malaise, hypotension, and bronchospasm, probably due to release of antigens from dying worms. For this reason, treatment courses may begin with a lower dosage, with escalation over the first 4 days of treatment. Single annual doses of diethylcarbamazine, alone or with ivermectin or albendazole may be as effective as longer courses of diethylcarbamazine Footnote 5.

IMMUNIZATION: None.

PROPHYLAXIS: Diethylcarbamazine Footnote 1Footnote 7Footnote 17, 2-drugs combinations (diethylcarbamazine-albendazole or ivermectine-albedazole) or diethylcarbamazine fortified salt Footnote 17. Mosquito nets and repellents are effective in preventing infective insect bites Footnote 4.

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: No reported cases of laboratory-acquired infections with Brugia spp.

SOURCES/SPECIMENS: Blood, lymphatic, ascitic, or pleural fluid, hydrocele fluid or chylous urine Footnote 2Footnote 5, infected mosquitoes Footnote 18.

PRIMARY HAZARDS: Ingestion of B. pahangi (potentially infective in humans) has been effective in causing infection in dogs Footnote 19, accidental parenteral inoculation, droplet exposure of mucous membrane and transmission by mosquitoes Footnote 20.

SPECIAL HAZARDS: Infected mosquitoes should be maintained in facilities which reasonably preclude the exposure of personnel or their escape to the outside Footnote 20.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes Footnote 22.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities Footnote 22.

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.

SECTION IX – REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: November 2011.

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright © Public Health Agency of Canada, 2011 Canada

REFERENCES

Footnote 1
McPherson, T., & Nutman, T. B. (2007). Filarial Nematodes. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical Microbiology (9th ed., pp. 2156-2165). Washington, D.C.: ASM press.
Footnote 2
Plorde, J. J. (2004). Tissue Nematodes. In K. J. Ryan, & C. G. Ray (Eds.), Sherris Medical Microbiology, an Introduction to Infectious Disease (4th ed., pp. 779-789). USA: McGraw-Hill.
Footnote 3
Araujo, A. C., Souto-Padron, T., & de Souza, W. (1993). Cytochemical localization of carbohydrate residues in microfilariae of Wuchereria bancrofti and Brugia malayi. The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society, 41(4), 571-578.
Footnote 4
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (2003). Parasitic Zoonoses. Zoonoses: Infectious Diseases Transmissible from Animals to Humans. (3rd ed., pp. 261-403). Washington, DC.: ASM press.
Footnote 5
Rosenthal, P. J. (2010). Protozoal & Helminthic Infections. In S. J. McPhee, & M. A. Papadakis (Eds.), Current Medical Diagnosis & Treatment (49th ed., pp. 1348-1389). U.S.A: Mc Graw Hill.
Footnote 6
Melrose, W. D. (2002). Lymphatic filariasis: New insights into an old disease. International Journal for Parasitology, 32(8), 947-960.
Footnote 7
Bockarie, M. J., Taylor, M. J., & Gyapong, J. O. (2009). Current practices in the management of lymphatic filariasis. Expert Review of Anti-Infective Therapy, 7(5), 595-605.
Footnote 8
EDESON, J. F., WHARTON, R. H., & LAING, A. B. (1960). A preliminary account of the transmission, maintenance and laboratory vectors of Brugia pahangi. Transactions of the Royal Society of Tropical Medicine and Hygiene, 54, 439-449.
Footnote 9
Harbut, C. L., & Orihel, T. C. (1995). Brugia beaveri: Microscopic morphology in host tissues and observations on its life history. Journal of Parasitology, 81(2), 239-243.
Footnote 10
Eberhard, M. L. (1984). Brugia lepori sp. N. (filarioidea: Onchocercidae) from rabbits (Sylvilagus aquaticus, S. floridanus) in Louisiana. Journal of Parasitology, 70(4), 576-579.
Footnote 11
Gregory, W. F., & Maizels, R. M. (2008). Cystatins from filarial parasites: Evolution, adaptation and function in the host-parasite relationship. International Journal of Biochemistry and Cell Biology, 40(6-7), 1389-1398.
Footnote 12
Smith, H. L. (2000). Investigating development of infective stage larvae of filarial nematodes. Front Biosci, 5, E95-E102.
Footnote 13
Supali, T., Djuardi, Y., Pfarr, K. M., Wibowo, H., Taylor, M. J., Hoerauf, A., Houwing-Duistermaat, J. J., Yazdanbakhsh, M., & Sartono, E. (2008). Doxycycline treatment of Brugia malayi-infected persons reduces microfilaremia and adverse reactions after diethylcarbamazine and albendazole treatment. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 46(9), 1385-1393. doi:10.1086/586753
Footnote 14
World Health Organization. (1993). Laboratory Biosafety Manual (2nd ed.)
Footnote 15
Wang, X., Jobe, M., Tyler, K. M., & Steverding, D. (2008). Efficacy of common laboratory disinfectants and heat on killing trypanosomatid parasites. Parasites and Vectors, 1(1)
Footnote 16
Pflug, I. J., Holcomb, R. G., & Gomez, M. M. (2001). Principles of the Thermal Destruction of Microorganisms. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 79-129). Philadelphia, USA: Lippincott Williams & Wilkins.
Footnote 17
World Health Organization. (2006). Global Programme to Eliminate Lymphatic Filariasis. Weekly Epidemiological Record, 22(81), 221-232.
Footnote 18
Herwaldt, B. L. (2006). Protozoa and Helminths. In D. O. Fleming, & D. L. Hunt (Eds.), Biological safety, Principles and practices (4th ed., pp. 115-161). Washington, D.C.: ASM Press.
Footnote 19
Bosworth, W., & Chernin, E. (1976). Oral transmission of Brugia pahangi to dogs. The American Journal of Tropical Medicine and Hygiene, 25(5), 762-764.
Footnote 20
US Department of Health and Human Services. (1999). Biosafety in Microbiological and Biomedical Laboratories. In J. Y. Richmond, & R. W. McKinney (Eds.), (4th ed., pp. 118). Washington, D.C.: U.S. Government Printing Office.
Footnote 21
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
Footnote 22
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.